ReviewFrontiers in immunology2021
IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 78 citations in OpenAlex.
- A skin-kidney neutrophil axis links ultraviolet exposure to renal angiogenesis and tissue remodeling in healthy and lupus kidneys.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- IL-18 Promotes the Development of Lupus Nephritis by Activating the Wnt/β-Catenin Signaling Pathway in Renal Tubular Epithelial Cells.Inflammation · 2026Article
- Decoding Lupus Diagnosis, Pathogenesis and Therapy: From Systemic Autoimmunity to Renal Damage.Diagnostics (Basel, Switzerland) · 2026Review
- The Evolution of Lupus Nephritis Therapy from the 1960s to the Present.Bioengineering (Basel, Switzerland) · 2026Review
- The Fibro-Immune Landscape Across Organs: A Single-Cell Comparative Study of Human Fibrotic Diseases.International journal of molecular sciences · 2026Article
- Identification and validation of key autophagy-related genes in Lupus nephritis.Clinical rheumatology · 2026Article
- Single-cell spatial transcriptomics reveals pathogenic mechanism of renal fibrosis in imiquimod-induced lupus nephritis in mice.Biochemistry and biophysics reports · 2025Article
- Taming renal inflammation: signaling pathways and therapeutic advances in lupus nephritis.BMC nephrology · 2025Review
- Spatially resolved transcriptomic profiling for glomerular and tubulointerstitial gene expression in C3 glomerulopathy.Clinical kidney journal · 2025Article
- Macrophage-Derived Type 1 IFN, Renal Tubular Epithelial Cell Polyploidization, and AKI-to-CKD Transition.Journal of the American Society of Nephrology : JASN · 2025Article
- Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2025Review
- Targeting the Type I Interferon Pathway in Glomerular Kidney Disease: Rationale and Therapeutic Opportunities.Kidney international reports · 2025Review
- Xian Huang Fang Inhibits the PKCδ/MAPK Signaling Pathway to Attenuate Renal Tubular Epithelial Cell Senescence and Thereby Delay Renal Interstitial Fibrosis.Drug design, development and therapy · 2025Article
- The Roles of RNA N6-methyladenosine Modifications in Systemic Lupus Erythematosus.Cell biochemistry and biophysics · 2024Review
- A Novel Preclinical Murine Model of Systemic Lupus Erythematosus-Like Cardiovascular Disease.ACR open rheumatology · 2024Article
- HDAC6 promotes inflammation in lupus nephritis mice by regulating transcription factors MAFF and KLF5 in renal fibrosis.Renal failure · 2024Article
- Expression of myxovirus resistance protein A in lupus nephritis and other glomerular nephropathies.Journal of nephrology · 2024Article
- TM9SF1 expression correlates with autoimmune disease activity and regulates antibody production through mTOR-dependent autophagy.BMC medicine · 2024Article
- STING-STAT6 Signaling Pathway Promotes IL-4Immune network · 2024Article
- SARS-CoV-2 spike aggravates lupus nephritis and lung fibrosis in systemic lupus erythematosus.Lupus science & medicine · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis (LN) is a common complication of systemic lupus erythematosus (SLE) and a major risk factor for morbidity and mortality. The abundant cell-free nucleic (DNA/RNA) in SLE patients, especially dsDNA, is a key substance in the pathogenesis of SLE and LN. The deposition of DNA/RNA-immune complexes (DNA/RNA-ICs) in the glomerulus causes a series of inflammatory reactions that lead to resident renal cell disturbance and eventually renal fibrosis. Cell-free DNA/RNA is the most effective inducer of type I interferons (IFN-I). Resident renal cells (rather than infiltrating immune cells) are the main source of IFN-I in the kidney. IFN-I in turn damages resident renal cells. Not only are resident renal cells victims, but also participants in this immunity war. However, the mechanism for generation of IFN-I in resident renal cells and the pathological mechanism of IFN-I promoting renal fibrosis have not been fully elucidated. This paper reviews the latest epidemiology of LN and its development process, discusses the mechanism for generation of IFN-I in resident renal cells and the role of IFN-I in the pathogenesis of LN, and may open a new perspective for the treatment of LN.
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